Corticotrophin and corticosterone secretion following Δ1-tetrahydrocannabinol, in intact and in hypothalamic deafferentated male rats

Puder, M.; Weidenfeld, Joseph; Chowers, I.; Nir, I.; Conforti, N.; Siegel, Richard A.

doi:10.1007/bf00238101

Cited by 48 publications

(27 citation statements)

References 21 publications

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“…However, other studies demonstrated an elevation in CORT level after administration of cannabinoid receptor agonist in experimental animals [23,24]. Moreover, some studies revealed that administration of cannabinoid receptor agonists activate the HPA axis [25][26][27][28]. In our study, pretreatment of mice with FAAH inhibitor, URB597, or anandamide transport inhibitor, AM404, significantly increased CORT level.…”

Section: Discussionmentioning

confidence: 43%

Cannabinoids and Their Interactions with Diazepam on Modulation of Serum Corticosterone Concentration in Male Mice

et al. 2009

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Experimental results indicate a mutual interaction between cannabinoidergic and GABAergic systems; however, the interaction between these systems on corticosterone release has not been fully investigated. In this study, we treated male mice with either cannabinoid compounds alone or in combination with diazepam. Blood samples were collected at 60 min post-injection. The serum corticosterone (CORT) level was measured using ELISA technique. Acute treatment of mice by cannabinoid receptor agonist WIN55212-2 (2.5 mg/kg; i.p.) resulted in a significant reduction of CORT, while treatment with either endocannabinoid reuptake inhibitor AM404 or endocannabinoid degradation enzyme inhibitor URB597 increased CORT compared to control group. Co-administration of AM404 or URB597 with cannabinoid CB1 receptor antagonist AM251 blocked the effect of these compounds on CORT. Treatment of mice with different doses of diazepam alone did not alter CORT compared to control group. However, co-administration of diazepam and either AM404 or WIN55212-2 significantly reduced CORT compared to the respective group treated with cannabinoid compound alone. Co-administration of ineffective dose of URB597 and ineffective dose of diazepam increased CORT level compared to groups treated with each compound alone. In conclusion, our findings suggest that the endogenous cannabinoid system is active as a modulator of CORT in mice and diazepam can alter the effect of cannabinoid system in the modulation of neuroendocrine functions.

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Section: Discussionmentioning

confidence: 43%

Cannabinoids and Their Interactions with Diazepam on Modulation of Serum Corticosterone Concentration in Male Mice

et al. 2009

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“…Early studies showed that peripherally administered THC stimulates ACTH secretion (Puder et al, 1982). Later studies showed that the cannabinoid receptors are expressed at the level of both the hypothalamus and pituitary (Herkenham et al, 1991), suggesting that the effects of cannabinoids on the HPA-axis are direct (i.e.…”

Section: Discussionmentioning

confidence: 98%

The role of endogenous cannabinoids in the hypothalamo-pituitary-adrenal axis regulation: in vivo and in vitro studies in CB1 receptor knockout mice

et al. 2004

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“…Animals with complete deafferentation of the medio-basal hypothalamus, with markedly depleted content of CRF-41 in the median eminence, did not respond to THC (100). In a recent study we showed that anandamide parallels THC in activating the HPA axis via mediation of a central mechanism which involves the secretion of CRF-41 (131).…”

Section: The Effect Of Hu-210 On the Hpa Axismentioning

confidence: 94%

Endogenous and Synthetic Cannabinoids: Recent Advances

et al. 1996

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In this review we present a summary of recent results on the action of cannabinoids endogenous to the central nervous system (CNS; the anandamides) and peripheral tissues (2-arachidonoyl-glycerol 2-Ara-GI), as well as two synthetic cannabinoids, HU-2 10, a highly potent cannabinoid agonist, and its enantiomer, HU-2 1 I , an N-methyl-D-aspartate (NMDA) antagonist that lacks cannabinoid activity.The major psychoactive constituent of Cannabis sativa, A9-tetrahydrocannabinol (THC), was first isolated in pure form and its structure elucidated by our group in 1964 (49). Shortly thereafter, its stereochemistry was established ( Fig. 1) (80), and several total syntheses were achieved (79,102). These advances and the public interest in Cannabis, in particular during the "flower years" of the 1960s and 197Os, led to extensive research that clarified to a large extent many aspects of cannabinoid action such as its metabolism, physiological and pharmacological effects, and various clinical and therapeutic aspects (28,74,85,99). It was not until 1988, however, that a major breakthrough in our understanding of the mode of action of cannabinoids was achieved with the identification and, shortly thereafter the cloning, of a cannabinoid receptor (now designated CB,) in brain and in neuroblastoma cells (25,76). In 1993 a second receptor (CB2) was found to be present in spleen (88). Various structural and biochemical aspects of CBI and CB2 have been reviewed in a recent book (98) and in detailed reviews (31,57,75). While CBI is found mostly in the brain, its RNA has also been detected in some peripheral tissues (21,2930). CB2 and its RNA have been detected only in cells of the immune system (39,88).

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Corticotrophin and corticosterone secretion following Δ1-tetrahydrocannabinol, in intact and in hypothalamic deafferentated male rats

Cited by 48 publications

References 21 publications

Cannabinoids and Their Interactions with Diazepam on Modulation of Serum Corticosterone Concentration in Male Mice

Cannabinoids and Their Interactions with Diazepam on Modulation of Serum Corticosterone Concentration in Male Mice

The role of endogenous cannabinoids in the hypothalamo-pituitary-adrenal axis regulation: in vivo and in vitro studies in CB1 receptor knockout mice

Endogenous and Synthetic Cannabinoids: Recent Advances

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